Table 1.

Potential inhibitors of NLRP3 inflammasome. NLRP3-specificity and targets (including the mode of action) are also represented.

Drug	NLRP3-Specific	Direct Inhibition	Action
Glyburide [17,69,70,71,72,73,74,75]	Yes	No	Induces the closure of ATP-sensitive K+ channels; Raises the intracellular K+ concentration
16673-34-0 [71,72]	Yes	No	Interferes with downstream events involved in NLRP3 conformational changes secondary to activation or binding to ASC
JC124 [76,77]	Yes	No	Blocks ASC aggregation, caspase-1 activation, and IL-1β secretion
FC11A-2 [78]	Yes	No	Repress IL-1β/18 release; induces autocleavage of procaspase-1, resulting in a reduced amount of activated caspase-1
MCC950 [79,80,81,82,83,84]	Yes	Yes	Blocks the release of IL-1β induced by NLRP3 activators
CY-09 [85,86,87]	Yes	Yes	Blocks the ATP, monosodium urate (MSU), and nigericin-induced activation of caspase-1 and resultant release of IL-1β
Tranilast [80,88,89,90]	Yes	Yes	Impairs the endogenous NLRP3-ASC interaction
OLT1177 [91,92]	Yes	Yes	Binds with NLRP3 to block its ATPase activity
Oridonin [93,94,95,96,97]	Yes	Yes	Inhibits the NF-κB or MAPK activation and repress the release of inflammasome-independent proinflammatory cytokines release
Parthenolide [98,99,100,101]	No	No	Inhibits caspase-1 activation; Targets ATPase activity of NLRP3
VX-740/VX-765 [102,103,104,105,106,107,108]	No	No	Block caspase-1 and resultant cleavage of pro-IL-1β/18
Bay 11-7082 [87,99]	No	No	Prevents the organization of ASC pyroptosome
BHB [109]	No	No	Lowered the production of IL-1ß and IL-1; reduces the oligomerization and speck formation of ASC